Date of Award

1-1-1985

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Biology

Abstract

The genetics and development of 5 embryo-lethal maize mutants defective in early embryogenesis were studied by genetic, histological, ultrastructural, and tissue culture techniques. The mutants examined were cp*-E1113A (dek22) on 1L, dcr*-E1428 (dek23) on 2L, rgh*-E1210, fl*-E1253B, and cp*-E1399A. They were found to be non-allelic. Long term studies of chromosome arm location by the Twaxy translocation stocks and mapping of cp*-E1113A and dcr*-E1428 with multiple linkage marker stocks were initiated. Three mutants lacked leaf primordia at kernel maturity, while two made leaf primordia but were unable to germinate. Embryos of cp*-E1113A became blocked at the transition stage but remained morphologically normal. Embryos of dcr*-E1428 became blocked at an abnormal coleoptilar stage. They were arrowhead-shaped and lacked a shoot apex. Necrosis appeared early in the shoot apex region and later spread through the embryo. Mutant embryos failed to make callus on auxin-containing media. Embryos of rgh*-E1210 became retarded by 8 days after pollination (DAP). At the transition stage (10 DAP) they began proliferative growth into irregular masses bearing meristematic lobes, and became blocked at an abnormal transition or coleoptilar stage. When cultured on auxin-containing media some rgh*-E1210 embryos produced embryogenic callus and somatic embryos displaying the rgh*-E1210 mutant phenotype. Embryos of fl*-E1253B developed to stage 2, but their differentiated structures underwent proliferation and loss of organization. Both rgh*-E1210 and fl*-E1253B showed reduced transmission of the mutant allele through pollen; the reduction in fl*-E1253B may be due to a linked gametophyte factor. Embryos of cp*-E1399A were normal in morphology but retarded in development, reaching stage 3 by kernel maturity. Mutant embryos were rescued on media supplemented with proline or abscisic acid.The mutants in this study are non-allelic. They differ in their stage of blockage, their capacity for morphogenesis, and their developmental patterns. This research indicates that this group of mutants represents 5 different gene loci, each playing a different, unique, and essential role in maize embryo development.

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